L-Arginine administration improves endothelium-dependent vasodilation and clinical symptoms in patients with cardiovascular disease, hypercholesterolemia, and atherosclerosis.
Does L-arginine improve endothelial function and clinical symptoms in patients with cardiovascular disease?
L-arginine administration improves endothelial function and clinical symptoms in cardiovascular disease, likely via nitric oxide synthase substrate provision.
L-Arginine (2-amino-5-guanidinovaleric acid) is the precursor of nitric oxide, an endogenous messenger molecule involved in a variety of endothelium-mediated physiological effects in the vascular system. Acute and chronic administration of L-arginine has been shown to improve endothelial function in animal models of hypercholesterolemia and atherosclerosis. L-Arginine also improves endothelium-dependent vasodilation in humans with hypercholesterolemia and atherosclerosis. The responsiveness to L-arginine depends on the specific cardiovascular disease studied, the vessel segment, and morphology of the artery. The pharmacokinetics of L-arginine have recently been investigated. Side effects are rare and mostly mild and dose dependent. The mechanism of action of L-arginine may involve nitric oxide synthase substrate provision, especially in patients with elevated levels of the endogenous NO synthase inhibitor asymmetric dimethylarginine. Endocrine effects and unspecific reactions may contribute to L-arginine-induced vasodilation after higher doses. Several long-term studies have been performed that show that chronic oral administration of L-arginine or intermittent infusion therapy with L-arginine can improve clinical symptoms of cardiovascular disease in man.
Böger et al. (Sun,) conducted a review in Cardiovascular disease, hypercholesterolemia, atherosclerosis. L-Arginine was evaluated. L-Arginine administration improves endothelium-dependent vasodilation and clinical symptoms in patients with cardiovascular disease, hypercholesterolemia, and atherosclerosis.